AB1506 PLASMA NEUROFILAMENT LIGHT CHAIN AND GLIAL FIBRILLARY ACIDIC PROTEIN AS BIOMARKERS IN PATIENTS WITH OCULAR SARCOIDOSIS AND NEUROSARCOIDOSIS
Authors: K. E. Byg, J. Grauslund, T. Ellingsen, J. Wied, L. Cehofski, J. Madsen, D. Olsen, H. Nielsen, T. Sejbaek
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Sarcoidosis is a disease characterized by non-caseating granulomatous inflammation, which can affect the eyes as ocular sarcoidosis (OS) and the central nervous system (CNS) as neurosarcoidosis (NS). Neurofilament light chain (NFL) is a structural neuronal cytoskeletal protein, and glial fibrillary acidic protein (GFAP) is part of the cytoskeleton in astrocytes and retinal Müller glial cells. Inflammation would cause leakage of NFL and GFAP. It has been demonstrated that plasma NFL is highly elevated in newly diagnosed NS patients with levels over 11.4 ng/L. <h3>Objectives</h3> The objectives were to compare the level of NFL and GFAP in sarcoidosis patients with or without OS and NS. <h3>Methods</h3> This cross-sectional study included 106 biopsy-verified chronic sarcoidosis patients examined between May and November 2019. After excluding 18 patients due to systemic comorbidity, the patients were divided according to their organ involvement over time: sarcoidosis without ocular or CNS affection (non-OS/non-NS, n=44), OS (n=14), NS (n=15), and combined OS and NS (n=15). EDTA plasma was stored at -80 ◦C until analysis. NFL and GFAP were measured blinded to clinical data by single molecule array technology (Simoa, HD-1 Analyser, Quanterix©, Billerica, MA, USA), using the commercially available 2-Plex assay. Kruskal–Wallis test, Dunn test, and Fisher's exact test were used for statistical analysis. <h3>Results</h3> We included 88 patients with an age median (IQR) of 52 years (41 - 60). The non-OS/non-NS group was younger than the other groups (p = 0.02) but did not differ with respect to disease duration (p=0.5). Between 67-100% of the patients received immunosuppressive treatment, most frequently in the OS group (93%) and the NS group (100%) (p = 0.02). Median NFL was 5.1, 8.4, 7.0, and 7.0 ng/L in patients with non-OS/non-NS, OS, NS, and combined OS and NS, respectively (p = 0.003), although this was only statistically significant in patients with a disease duration &lt; 5 years (p = 0.005). The frequency of patients with an NFL level &gt;11.4 ng/L was lower in non-OS/non-NS group compared to the three other groups (2% vs. 14% vs. 33% vs. 20%, p = 0.004). There was a trend (p = 0.06) towards a lower median GFAP in patients with non-OS/non-NS as compared to the other groups (52 vs. 72 vs. 71 vs. 69 ng/L), which became statistically significant in patients with a disease duration &lt; 5 years (48 vs. 67 vs. 127 vs. 52 ng/L, p = 0.02). <h3>Conclusion</h3> In this cross-sectional study of chronic sarcoidosis patients, we generally found a low median NFL level, including in OS and NS patients. Our results suggest that neuroaxonal damage and, thereby, active inflammation decreases in treated sarcoidosis patients. However, the median NFL levels were significantly lowest in the non-OS/non-NS group, and between 14-33% of patients in OS, NS, and combined OS and NS groups had an NFL level above 11.4 ng/l, which could indicate active CNS inflammation leading to ongoing silent neuroaxonal damage. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.